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I write about the excellent article describing studies of patients with dilated cardiomyopathy who were treated with Trimetazidine.1 The apparent beneficial effect of this agent on left ventricular ejection fraction in patients with congestive heart failure has been demonstrated previously.2 The current report describes metabolic and hormonally related factors that may in part explain the mechanisms of action of the drug.

It is of interest that over the 3-month treatment period the recipient group demonstrated increased left ventricular mass whereas the placebo control group did not. The mechanism is unclear, particularly in view of the decrease in left ventricular wall stress in the treated subjects. This suggests that the agent has a primary effect on the myocyte. Trimetazidine has been shown to inhibit cardiomyocyte apoptosis in an ischemia reperfusion model.3 However, if apoptosis was the cause for the different left ventricular mass effects in the 2 groups, one might have expected the control hearts to demonstrate atrophy over time, which they did not.

Whatever the mechanism, if hypertrophy can be confirmed in patients treated with trimetazidine, it will be important to determine the nature of the hypertrophy and whether it is beneficial or deleterious. The authors are to be congratulated on conducting a difficult study and beginning to explore mechanisms of action in humans of a potentially important therapeutic agent.